PMID- 10818152
OWN - NLM
STAT- MEDLINE
DCOM- 20000615
LR  - 20191023
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 20
IP  - 11
DP  - 2000 Jun 1
TI  - Insulin-like growth factor I stimulates dendritic growth in primary somatosensory 
      cortex.
PG  - 4165-76
AB  - The temporal and spatial distributions of several growth factors suggest roles in 
      the regulation of neuronal differentiation in the neocortex. Among such growth 
      factors, the insulin-like growth factors (IGF-I and -II) are of particular 
      interest because they are available to neurons from multiple sources under 
      independent control. IGF-I is produced by many neurons throughout the brain and 
      also by cells in the cerebral vasculature. IGF-II is found at high levels in the 
      CSF, and both IGF-I and IGF-II cross the blood-brain barrier. Thus, the IGFs may 
      act as both paracrine and endocrine regulators of neuronal development. As an 
      initial step toward understanding the influence of IGFs in the developing 
      cerebral cortex, the present study examined the effects of IGF-I and of the 
      neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) 
      on the dendritic complexity of layer 2 pyramidal neurons. The results demonstrate 
      that IGF-I increased the branching and total extent of both apical and basal 
      dendrites of pyramidal cells in organotypic slices of rat primary somatosensory 
      cortex. BDNF and NT-3 also enhanced dendritic development, but the two 
      neurotrophins increased the extent of only basal, not apical, dendrites and 
      promoted greater elongation than was seen after IGF-I treatment. These results 
      provide direct evidence that IGF-I can regulate the dendritic elaboration of 
      cortical neurons and indicate that endogenous IGFs may influence dendritic 
      differentiation and the formation of cortical connections. In addition, 
      IGF-dependent regulation of dendritic structure may represent a link between 
      age-related declines in IGFs and cognitive deficits seen in senescence.
FAU - Niblock, M M
AU  - Niblock MM
AD  - Department of Neurobiology and Anatomy and Program in Neuroscience, Wake Forest 
      University School of Medicine, Winston-Salem, North Carolina 27157-1010, USA.
FAU - Brunso-Bechtold, J K
AU  - Brunso-Bechtold JK
FAU - Riddle, D R
AU  - Riddle DR
LA  - eng
GR  - P01 AG011370/AG/NIA NIH HHS/United States
GR  - 1 PO1 AG 11370/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Neurotrophin 3)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Cell Count
MH  - Cell Size
MH  - Dendrites/*drug effects/ultrastructure
MH  - Female
MH  - Image Processing, Computer-Assisted
MH  - Insulin-Like Growth Factor I/*pharmacology
MH  - Neurotrophin 3/pharmacology
MH  - Organ Culture Techniques
MH  - Pyramidal Cells/drug effects/ultrastructure
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Somatosensory Cortex/cytology/drug effects/*growth & development
MH  - Stimulation, Chemical
PMC - PMC6772633
EDAT- 2000/05/20 00:00
MHDA- 2000/06/17 00:00
PMCR- 2000/12/01
CRDT- 2000/05/20 00:00
PHST- 2000/05/20 00:00 [pubmed]
PHST- 2000/06/17 00:00 [medline]
PHST- 2000/05/20 00:00 [entrez]
PHST- 2000/12/01 00:00 [pmc-release]
AID - 20/11/4165 [pii]
AID - 4191 [pii]
AID - 10.1523/JNEUROSCI.20-11-04165.2000 [doi]
PST - ppublish
SO  - J Neurosci. 2000 Jun 1;20(11):4165-76. doi: 10.1523/JNEUROSCI.20-11-04165.2000.